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Expression of the rel-A component of nuclear factor κ B (NFκB) by human endometrial cells was investigated by immunocytochemical analysis of cryostat sections cut from endometrial biopsy material and of cultured endometrial epithelial cells. In-vivo expression of rel-A was low in epithelial cells in endometrium obtained during the proliferative phase of the cycle, but increased in these cells during the secretory phase and was maximal at the time of implantation. In-vivo expression of rel-A by stromal cells did not vary greatly throughout the cycle, but showed a slight peak at the time of ovulation. In contrast similar expression of rel-A was seen in short-term cultures of epithelial cells prepared from both proliferative and secretory endometrium. Addition of the NFκB inhibitor SN50 (5 μg/ml) to confluent cultures of endometrial epithelial cells inhibited interleukin (IL)-1α (10 ng/ml) and tumour necrosis factor α (TNFα) (10 ng/ml) stimulated IL-6 (P < 0.001 and P < 0.01 respectively) and LIF (P < 0.01 and P < 0.05 respectively) production. The proteasome inhibitor MG132 (0.3 and 3 μmol/l) also caused a dose-dependent decrease in IL-1α and TNFα-stimulated IL-6 (P < 0.001 and P < 0.001 respectively) and leukaemia inhibitory factor (LIF) (P < 0.001 and P < 0.001 respectively) production by endometrial epithelial cells. The results support the hypothesis that NFκB mediates signalling between IL-1 and TNFα receptors and the expression of LIF and IL-6 in endometrial epithelial cells. [ABSTRACT FROM AUTHOR]

The production of tumour necrosis factor a (TNF-α) by cultured human endometrial epithelial and stromal cells prepared from endometrium obtained at different stages in the menstrual cycle has been investigated. TNF-α was not detectable in the supernatants of stromal cell cultures prepared from endometrial tissue obtained at any time in the menstrual cycle. TNF-α production by endometrial epithelial cells in culture varied depending on the time in the cycle at which the endometrial tissue was taken. Cells prepared from tissue obtained during the late proliferative phase of the cycle produced more TNF-α than those prepared from tissue obtained at other times in the cycle. In addition, a small increase in TNF-α production was seen by cells prepared from tissue obtained during the mid-secretory phase of the cycle. Interieukin 1 (IL-1) (1.4–140 pmol/1) caused a dose-dependent increase in TNF-α production by cells prepared from both proliferative and secretory endometrium. Maximum LL-1-stimulated increases in TNF-α production were similar in cells from both proUferative and secretory endometrium and typically reached from four to 10 times basal values. High doses of progesterone, either alone or in the presence of oestradiol, also affected TNF-a production by epithelial cells. TNF-α production by cells prepared from proliferative endometrium was increased by progesterone. In contrast, TNF-α production by cells prepared from secretory endometrium was decreased in the presence of progesterone. The effects of steroids on TNF-α production were less marked than that of IL-1, with values increasing or decreasing to a maximum of three times the basal value. Placental protein 14 (PP14) (0.18 and 1.8 nmol/1) also increased TNF-α production by cells prepared from proliferative tissue, but had no effect on its production by cells prepared from secretory endometrium. PP14-stimulated TNF-α levels typically only reached a maximum of two times basal values. [ABSTRACT FROM PUBLISHER]